Women with Polycystic Ovary (PCO) syndrome have characteristics including anovulation, hyperandrogenism and insulin resistance, which suggest a male CHD risk factor profile. Since the last submission, the investigators have recruited and screened 244 women with PCO syndrome and 244 age matched neighborhood controls. In addition, as part of a minority recruitment effort they have identified and screened 71 non-white women who met the criteria for the study. The overall response rate was 84.5%. It was determined that women with this condition have significantly elevated CHD risk factors at an early age. These include: increased BMI, LDL, and triglycerides (P<.001), decreased HDLT and HDL2 (p<.01), increase waist-hip ratio, fasting insulin, and systolic blood pressure (p<.05). There is also evidence that the LDL cholesterol is increased at an early age in PCO participants but does not increase dramatically with age as is that case among non-PCO women. The investigators now propose to investigate whether women with PCO syndrome (PCOS) have evidence of an increased prevalence rate of subclinical atherosclerosis as measured by the presence of plaque, increased intima-medial carotid artery wall thickness and lower brachial artery flow mediated vasodilation. Within the PCOS population they will further determine risk factors for subclinical atherosclerosis. Thus, the specific aims are as follow. 1) Evaluate the relationship between PCOS and subclinical atherosclerosis as measured by carotid ultrasound. They will determine whether women >=30 years of age with PCOS have a higher prevalence of subclinical atherosclerosis than age-matched control women (N=150 cases, 150 controls). 2) Evaluate the relationship between PCOS and subclinical vascular disease as measured by brachial artery flow mediated vasodilation. They will determine whether PCOS cases have lower brachial artery flow mediated vasodilation than controls, and whether the distribution of flow mediated vasodilation is related to the extent of carotid artery wall thickness and plaque (n=150 cases, 150 controls). 3) Evaluate whether subclinical atherosclerosis and vascular disease are related to the following cardiovascular risk factors within PCOS cases and controls: HDLc, LDLc, triglycerides, insulin, systolic and diastolic blood pressure and testosterone, waist-to-hip ratio and body mass index (BMI). 4) Evaluate differences in body composition between PCOS cases and control women. Two aspects of body composition will be assessed: intra-abdominal fat as measured by computed tomography (CT) of the abdomen, sagittal diameter and percent body fat as measured by dual energy x-ray absorptiometry (DEXA). They will evaluate the relationship between subclinical atherosclerosis and body composition separately for cases and for controls. Previous studies have clearly shown that PCOS women are different from obese non-PCOS women. Moreover, insulin, testosterone and CHD risk factors will also be correlated with these measures using paired t-tests. Multiple regression will be used to test whether PCO cases compared to controls have an increase in intra-abdominal fat which is independent of important confounders. Finally, they will 5) compare plasma levels of selected coagulation factors including fibrinogen and factor VII to fibrinolytic factors for PCOS cases and controls.